Explaining Osteomyelitis and Prosthetic Joint Infections (PJI) in terms of Biofilm – A Review

@#Osteomyelitis is a chronic infection of bones. Eradication of bone infection is usually with antibiotics and debridement, but it is slow and the infection can recur even after many years. It is now established that osteomyelitis is due to biofilm and a better understanding of the process is required. We review the development of biofilm and apply it to osteomyelitis management. The planktonic microbes' response to adverse conditions is the formation of biofilm. Bacterial infections in planktonic forms cause infections that can be controlled with antibiotics and immunisation, however the same microbe when its phenotype becomes biofilm is more resilient. The understanding of how planktonic bacteria convert to biofilm is one of the aims set out for this article.

Fulvestrant inhibits the glycolysis of prolactinoma GH3 cells by downregulating IRE1/XBP1 signaling pathway.

OBJECTIVE: We aimed to evaluate the effects of fulvestrant on the glycolysis of prolactinoma GH3 cells, and reveal the potential regulatory mechanisms. MATERIALS AND METHODS: Prolactinoma cell line GH3 was treated with different concentrations of fulvestrant (0, 0.12, 0.25, 0.5 and 1 ng/ml) for 4 h. siRNAs XBP1s and XBP1u were constructed to treat GH3 cells. The expression levels of XBP1s, XBP1u, IRE1, PKM2 and GRP78 of GH3 cells were detected by Western blot. Meanwhile, the glycolytic activity of GH3 cells, including the glucose uptake, ATP/ADP, and lactate production were detected. RESULTS: The expression levels of XBP1s and XBP1u were significantly inhibited by fulvestrant in a dose-dependent manner. The glucose uptake, ATP/ADP and lactate production of GH3 cells were significantly inhibited by fulvestrant as well as siRNA XBP1s and XBP1u (p < 0.05). Western blot analysis suggested that the expression levels of IRE1, PKM2 and GRP78 were significantly decreased in GH3 cells treated by fulvestrant as well as siRNA XBP1s and XBP1u, compared with those in normal control (p < 0.05). CONCLUSIONS: Fulvestrant could inhibit the glycolysis of GH3 cells by downregulating IRE1/XBP1 signaling pathway, and this process was closely related with the downregulation of PKM2.

Adherence To Acne Medication And Its Relation To Acne Severity And Quality Of Life

Background: Acne vulgaris is a chronic condition which commonly affects adolescents and exerts a psychological burden on its sufferers. Non-adherence to acne treatment is believed to be a major factor contributing to treatment failure. In this study, we characterize the profile of a non-adherent Asian acne patient, and evaluate the relationship between treatment adherence and acne severity and quality of life. Methods: A total of 53 acne patients were recruited from the Dermatology outpatient clinic of National University Hospital, Singapore, and followed up over a 3 month period in this prospective observational study. The Elaboration d’un outil d’evaluation de l’observance (ECOB) adherence assessment tool was used to assess adherence to acne treatment, and acne severity was evaluated using the US Food and Drug Administration Center 5-point Acne Severity Score (ASS). Results: Of the 53 study participants, 29 (54.7%) were non-adherent to acne treatment. There was no significant difference in gender, educational level or acne severity at time of presentation between adherent and non-adherent patients. Adherent patients had a significantly larger improvement in acne severity scores compared to non-adherent patients (change in ASS: -1.33 ± 0.64 vs -0.76 ± 0.83, p = 0.008), but this did not translate to a significant improvement in quality of life. Conclusion: Adherence to acne treatment was not associated with demographic characteristics or acne severity. Factors contributing to adherence to acne treatment are complex and multi-faceted, and individualized motivation and education of each patient may be the method of choice in encouraging treatment adherence.